Journal
CELL HOST & MICROBE
Volume 21, Issue 6, Pages 695-+Publisher
CELL PRESS
DOI: 10.1016/j.chom.2017.05.012
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Funding
- NIH [U19 AI106761, R01 AI076327, T21-CA009537]
- Paul G. Allen Family Foundation
- NIH Tetramer Core Facility [HHSN272201300006C]
- European Developing Countries Clinical Trials Partnership (EDC TP) [IP.2007.32080.001]
- Statens Serum Institut
- European Commission [H2020-PHC-643381]
- Bill and Melinda Gates Foundation (BMGF) Global Health grant [OPP1066265]
- Bank of America Dissertation Fellowship
- Carnegie Corporation of New York
- Bill and Melinda Gates Foundation [OPP1066265] Funding Source: Bill and Melinda Gates Foundation
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CD4 T cells are critical for protective immunity against Mycobacterium tuberculosis (Mtb), the cause of tuberculosis (TB). Yet to date, TB vaccine candidates that boost antigen-specific CD4 T cells have conferred little or no protection. Here we examined CD4 T cell responses to two leading TB vaccine antigens, ESAT-6 and Ag85B, in Mtb-infected mice and in vaccinated humans with and without underlying Mtb infection. In both species, Mtb infection drove ESAT-6-specific T cells to be more differentiated than Ag85B-specific T cells. The ability of each T cell population to control Mtb in the lungs of mice was restricted for opposite reasons: Ag85B-specific T cells were limited by reduced antigen expression during persistent infection, whereas ESAT-6-specific T cells became functionally exhausted due to chronic antigenic stimulation. Our findings suggest that different vaccination strategies will be required to optimize protection mediated by T cells recognizing antigens expressed at distinct stages of Mtb infection.
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